Porphyria cutanea tarda (PCT) is recognized worldwide as the most common form of human porphyria. The photocutaneous disorder is caused by porphyrin overproduction in the liver which relates to diminished activity of uroporphyrinogen decarboxlase (UROD). The metabolic lesion almost invariable requires iron overload for its clinical and biochemical expression. We propose to evaluate the key role of iron in genesis of